NURS 5315 Advance Pathophysiology - Exam 3 - UTA
Mitral Valve Stenosis - Characterized by NARROWING of mitral valve
- Normal is 4-6 cm
-Narrowed is less than 2.5 cm
- Caused by RHEUMATIC FEVER
-More common in WOMEN
-Oxygenated blood comes back into heart into the left atrium and down through the
mitral valve to the left ventricle
- Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial
hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation
& causes PULMONARY EDEMA
- Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood
backs up into the left atrium and causes it to swell, then backs up into the lung and
causes resp. symptoms
-S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension
Mitral Valve Regurgitation -Characterized by INCOMPLETE CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly,
leaving valve ajar); more common in WOMEN; STICKING CHEST PAIN
-Blood in left ventricle backs up to left ventricle during systole (mitral valve should
be closed during systole/contraction of heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary vascular
pressure/volume, PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds
Aortic Valve Stenosis -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION (stiffening) in people over
60; congenital aortic valve stenosis in people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe when valve
is less than 0.5 cm
-Narrowed valve prevents outflow from left ventricle to aorta. This backs up blood to
the left atrium and ultimately floods the lung causing PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta sends
out oxygenated blood to body), causing fainting or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood properly to the body,
depriving tissues of oxygen. Blood gets backed up into lungs, causing pulmonary
edema.
Aortic Valve Regurgitation -Valve is TOO WIDE or TOO NARROW, blood doesn't pass through effectively,
causing back flow of blood into the left ventricle
-Marked by EARLY DIASTOLIC MURMUR (on systole, heart contracts and pushes
blood up the aorta, but on diastole, heart relaxes and ineffective aortic valve is not
able to hold blood up in aorta, so blood falls and makes a swish sound, which is the
murmur)
-Most commonly caused by AORTIC ROOT DILATION(starting point of aorta is too
wide)
-Other causes: infective endocarditis, rheumatic fever, aortitis from syphilis,
coarctation (congenital narrowing of aorta), aortic dissection (tear), ankylosing
spondylitis (inflammatory arthritis)
-Acute: increases left ventricular end-diastolic pressure (LVEDP) (increased blood
back down in the left ventricle increases pressure), decreased stroke volume (not
much blood is being pushed from left ventricle because blood's backed up and
overwhelming left ventricle), normal or decreased pulse pressure, decreased
cardiac output (aorta is not effectively pumping blood from heart)
Chronic: Body adjusts; LVEDP normalizes, systolic bp increases (compensation:
harder contraction to push blood out of aorta before it falls back down to left
ventricle), diastolic bp decreases (compensation: decreased relaxation of heart to
stop blood from seeping back out of aorta), cardiac output is normal, pulse pressure
is increase. Blood ultimately is backed up into the left atrium and pulmonary
circulation.
Atherosclerosis Causes -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel, initiating
an inflammatory response)
, NURS 5315 Advance Pathophysiology - Exam 3 - UTA
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory 1. Tissue injury to endothelial cells lining the blood vessel.
Response 2. Endothelial cells become inflammed and unable to produce sufficient
antithrombotic and vasodilating cytokines, increasing risk for clot formation and
creating a tighter space for plaques and clots to grow.
3. Macrophages and platelets are called to the area of injury, further congesting the
growing plaque area.
4. LDL replaces endothelial cells in the lining of the blood vessel.
5. Macrophages engulf the LDL particles.
6. Macrophages eat too much LDL, causing them to burst and become foam cells
(under a microscope they look like sea foam)
7. Accumulation of foam cells causes a fatty streak. Fatting streak further triggers
inflammatory responses, repeating the whole cycle, and growing the fatty streak.
8. Smooth muscle hyperplasia from all the inflammation grows, produces collagen,
and covers the fatty streak to create a fibrous plaque.
9. The plaque may calcify, protrude into the vessel, and occlude blood flow,
resulting in ischemia or infarction.
Hyperlipidemia Leading cause of coronary artery disease
Most commonly affects promximal portions of coronary arteries, larger branches of
carotid arteries, circle of Willis (base of brain), large vessels of lower extremities,
renal arteries, mesenteric (intestinal) arteries
Consequences of Atherosclerosis Reduced blood flow
Coronary artery disease, myocardial infarction, carotid artery disease, cerebral
vascular disease, stroke, mesenteric ischemia, peripheral vascular disease, renal
artery stenosis
Congenital Heart Disease -Most common heart disease affecting children
-Etiology is unknown in 90% of cases
Causes:
Genetic/environmental factors (multifactorial factors)
Primary genetic factors (single gene disorders, chromosome disorders)
Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella
infection)
Maternal Risk Factors:
Age over 45, prior child with heart defect, poorly controlled diabetes during
pregnancy, alcohol, congenital infection during pregnancy (rubella), aspirin, lupus,
Dilantin/phenytoin/diphenylhydantoin for seizures
LEFT to RIGHT shunt (Congenital heart defect) -Oxygenated blood from the left side of the heart mixes with unoxygenated blood in
the right side of the heart.
-Oxygen saturation on left side is usually 95%, whereas right side is 75%
- As blood mixes, right side's oxygen saturation increases to 80% or more
-VOLUME OVERLOAD occurs on RIGHT side of heart occurs, leading to
PULMONARY HYPERTENSION, which causes RIGHT VENTRICULAR
HYPERTROPHY, (secondary to pulm. hptn.), and LEFT VENTRICULAR
HYPERTROPHY(secondary to blood being returned to left ventricle)
Eisenmenger Syndrome: Reversal of left to right shunt to a right to left shunt.
Eisenmenger Syndrome 1. Increased blood flow returns to lungs rather than to the rest of the body.
2. Blood vessels become stiff and narrow - permanent damage.
3. Increased pressure of the blood flow in the lung becomes so great that the
direction of blood flow through the shunt reverses.
4. Oxygen-poor (blue) blood from the right side of the heart flows into the left
ventricle and is pumped to the body and tissues do not receive enough oxygen.
5. Results in late-onset cyanosis (as in, later in life) and clubbing of fingernails.
Ventricular Septal Defect -Hole allowing blood to move from left ventricle to the right ventricle
(most common congenital heart defect) -Sign: Harsh holosytolic murmur at the lower left sternal border (high-pitched,
begins at the first heart sound (S1) and continue to the second heart sound (S2))
-Multiple VSDs are associated with Tetralogy of Fallot, Cri du Chat Syndrome, and
Fetal Alcohol Syndrome.
-Associated with development of atrial septal defects, patent ductus arteriosus,
coarction (congenital narrowing) of aorta, aortic valve stenosis, INCREASED RISK
FOR DEVELOPING ENDOCARDITIS at some point in life ( infection of the heart's
inner lining, usually involving the heart valves)
, NURS 5315 Advance Pathophysiology - Exam 3 - UTA
Atrial Septal Defect -Most common cause is a patent foramen ovale (hole) that does not close
(most common congenital heart defect in adults) -Associated with FETAL ALCOHOL SYNDROME and DOWN SYNDROME
-Sign: Midsystolic murmur at upper sternal border
-Increases risk for EMBOLUS
Patent Ductus Arteriosus Patent ductus arteriosus (PDA) is a persistent opening between the two major blood
vessels leading from the heart. The opening, called the ductus arteriosus, is a
normal part of a baby's circulatory system before birth that usually closes shortly
after birth. If it remains open, however, it's called a patent ductus arteriosus.
Sign: Machine-like murmur heard continuously throughout systole and diastole
Reversal may occur if pulmonary hptn occurs from increased blood flow through the
pulmonary artery. If this happens, unoxygenated blood will enter the aorta below the
level of the subclavian artery and the child will be cyanotic in the lower body, but not
in the upper body.
Associated with congenital rubella, Tetralogy of Fallot, respiratory distress
syndrome, and transposition of great vessels (unoxygenated blood does not pick up
oxygen in lungs and is pumped back to body)
Right to left shunt Tetralogy of Fallot is most common cyanotic congenital heart defect.
Impaired gas exchanged r/t decreased pulmonary blood flow
Right side of heart = Deoxygenated
Left side = Oxygenated
1. Deoxygenated blood is mixed with oxygenated blood.
2. Blood on left side has oxygen saturation decrease from 95% to 80% or lower.
3. Cyanosis may or may not develop depending on how low the oxygen saturation
on the left side drops.
-Left side oxygen saturation 85% or high, cyanosis is not likely to occur.
-Left side oxygen saturation below 80% is indicative of a large amount of blood
being shunted and will result in cyanosis.
Tetralogy of Fallot Most common cyanotic congenital heart defect
Tetralogy of Fallot involves four heart defects:
1. A large ventricular septal defect
2. Pulmonary stenosis
3. Right ventricular hypertrophy
4. An overriding aorta
Heart Failure Risk Factors -Age (most common over 65 y/o)
-Ischemic heart disease
-Obesity
-Diabetes
-Hypertension
-Excessive ETOH use
-Congenital heart disease
-Valvular heart disease
-Myocarditis
-Cardiomyopathy (stiffening of heart muscle)
-Renal failure
Heart Failure Clinical Manifestations -Volume overload
-Poor perfusion secondary to pump failure
Mitral Valve Stenosis - Characterized by NARROWING of mitral valve
- Normal is 4-6 cm
-Narrowed is less than 2.5 cm
- Caused by RHEUMATIC FEVER
-More common in WOMEN
-Oxygenated blood comes back into heart into the left atrium and down through the
mitral valve to the left ventricle
- Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial
hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation
& causes PULMONARY EDEMA
- Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood
backs up into the left atrium and causes it to swell, then backs up into the lung and
causes resp. symptoms
-S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension
Mitral Valve Regurgitation -Characterized by INCOMPLETE CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly,
leaving valve ajar); more common in WOMEN; STICKING CHEST PAIN
-Blood in left ventricle backs up to left ventricle during systole (mitral valve should
be closed during systole/contraction of heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary vascular
pressure/volume, PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds
Aortic Valve Stenosis -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION (stiffening) in people over
60; congenital aortic valve stenosis in people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe when valve
is less than 0.5 cm
-Narrowed valve prevents outflow from left ventricle to aorta. This backs up blood to
the left atrium and ultimately floods the lung causing PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta sends
out oxygenated blood to body), causing fainting or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood properly to the body,
depriving tissues of oxygen. Blood gets backed up into lungs, causing pulmonary
edema.
Aortic Valve Regurgitation -Valve is TOO WIDE or TOO NARROW, blood doesn't pass through effectively,
causing back flow of blood into the left ventricle
-Marked by EARLY DIASTOLIC MURMUR (on systole, heart contracts and pushes
blood up the aorta, but on diastole, heart relaxes and ineffective aortic valve is not
able to hold blood up in aorta, so blood falls and makes a swish sound, which is the
murmur)
-Most commonly caused by AORTIC ROOT DILATION(starting point of aorta is too
wide)
-Other causes: infective endocarditis, rheumatic fever, aortitis from syphilis,
coarctation (congenital narrowing of aorta), aortic dissection (tear), ankylosing
spondylitis (inflammatory arthritis)
-Acute: increases left ventricular end-diastolic pressure (LVEDP) (increased blood
back down in the left ventricle increases pressure), decreased stroke volume (not
much blood is being pushed from left ventricle because blood's backed up and
overwhelming left ventricle), normal or decreased pulse pressure, decreased
cardiac output (aorta is not effectively pumping blood from heart)
Chronic: Body adjusts; LVEDP normalizes, systolic bp increases (compensation:
harder contraction to push blood out of aorta before it falls back down to left
ventricle), diastolic bp decreases (compensation: decreased relaxation of heart to
stop blood from seeping back out of aorta), cardiac output is normal, pulse pressure
is increase. Blood ultimately is backed up into the left atrium and pulmonary
circulation.
Atherosclerosis Causes -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel, initiating
an inflammatory response)
, NURS 5315 Advance Pathophysiology - Exam 3 - UTA
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory 1. Tissue injury to endothelial cells lining the blood vessel.
Response 2. Endothelial cells become inflammed and unable to produce sufficient
antithrombotic and vasodilating cytokines, increasing risk for clot formation and
creating a tighter space for plaques and clots to grow.
3. Macrophages and platelets are called to the area of injury, further congesting the
growing plaque area.
4. LDL replaces endothelial cells in the lining of the blood vessel.
5. Macrophages engulf the LDL particles.
6. Macrophages eat too much LDL, causing them to burst and become foam cells
(under a microscope they look like sea foam)
7. Accumulation of foam cells causes a fatty streak. Fatting streak further triggers
inflammatory responses, repeating the whole cycle, and growing the fatty streak.
8. Smooth muscle hyperplasia from all the inflammation grows, produces collagen,
and covers the fatty streak to create a fibrous plaque.
9. The plaque may calcify, protrude into the vessel, and occlude blood flow,
resulting in ischemia or infarction.
Hyperlipidemia Leading cause of coronary artery disease
Most commonly affects promximal portions of coronary arteries, larger branches of
carotid arteries, circle of Willis (base of brain), large vessels of lower extremities,
renal arteries, mesenteric (intestinal) arteries
Consequences of Atherosclerosis Reduced blood flow
Coronary artery disease, myocardial infarction, carotid artery disease, cerebral
vascular disease, stroke, mesenteric ischemia, peripheral vascular disease, renal
artery stenosis
Congenital Heart Disease -Most common heart disease affecting children
-Etiology is unknown in 90% of cases
Causes:
Genetic/environmental factors (multifactorial factors)
Primary genetic factors (single gene disorders, chromosome disorders)
Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella
infection)
Maternal Risk Factors:
Age over 45, prior child with heart defect, poorly controlled diabetes during
pregnancy, alcohol, congenital infection during pregnancy (rubella), aspirin, lupus,
Dilantin/phenytoin/diphenylhydantoin for seizures
LEFT to RIGHT shunt (Congenital heart defect) -Oxygenated blood from the left side of the heart mixes with unoxygenated blood in
the right side of the heart.
-Oxygen saturation on left side is usually 95%, whereas right side is 75%
- As blood mixes, right side's oxygen saturation increases to 80% or more
-VOLUME OVERLOAD occurs on RIGHT side of heart occurs, leading to
PULMONARY HYPERTENSION, which causes RIGHT VENTRICULAR
HYPERTROPHY, (secondary to pulm. hptn.), and LEFT VENTRICULAR
HYPERTROPHY(secondary to blood being returned to left ventricle)
Eisenmenger Syndrome: Reversal of left to right shunt to a right to left shunt.
Eisenmenger Syndrome 1. Increased blood flow returns to lungs rather than to the rest of the body.
2. Blood vessels become stiff and narrow - permanent damage.
3. Increased pressure of the blood flow in the lung becomes so great that the
direction of blood flow through the shunt reverses.
4. Oxygen-poor (blue) blood from the right side of the heart flows into the left
ventricle and is pumped to the body and tissues do not receive enough oxygen.
5. Results in late-onset cyanosis (as in, later in life) and clubbing of fingernails.
Ventricular Septal Defect -Hole allowing blood to move from left ventricle to the right ventricle
(most common congenital heart defect) -Sign: Harsh holosytolic murmur at the lower left sternal border (high-pitched,
begins at the first heart sound (S1) and continue to the second heart sound (S2))
-Multiple VSDs are associated with Tetralogy of Fallot, Cri du Chat Syndrome, and
Fetal Alcohol Syndrome.
-Associated with development of atrial septal defects, patent ductus arteriosus,
coarction (congenital narrowing) of aorta, aortic valve stenosis, INCREASED RISK
FOR DEVELOPING ENDOCARDITIS at some point in life ( infection of the heart's
inner lining, usually involving the heart valves)
, NURS 5315 Advance Pathophysiology - Exam 3 - UTA
Atrial Septal Defect -Most common cause is a patent foramen ovale (hole) that does not close
(most common congenital heart defect in adults) -Associated with FETAL ALCOHOL SYNDROME and DOWN SYNDROME
-Sign: Midsystolic murmur at upper sternal border
-Increases risk for EMBOLUS
Patent Ductus Arteriosus Patent ductus arteriosus (PDA) is a persistent opening between the two major blood
vessels leading from the heart. The opening, called the ductus arteriosus, is a
normal part of a baby's circulatory system before birth that usually closes shortly
after birth. If it remains open, however, it's called a patent ductus arteriosus.
Sign: Machine-like murmur heard continuously throughout systole and diastole
Reversal may occur if pulmonary hptn occurs from increased blood flow through the
pulmonary artery. If this happens, unoxygenated blood will enter the aorta below the
level of the subclavian artery and the child will be cyanotic in the lower body, but not
in the upper body.
Associated with congenital rubella, Tetralogy of Fallot, respiratory distress
syndrome, and transposition of great vessels (unoxygenated blood does not pick up
oxygen in lungs and is pumped back to body)
Right to left shunt Tetralogy of Fallot is most common cyanotic congenital heart defect.
Impaired gas exchanged r/t decreased pulmonary blood flow
Right side of heart = Deoxygenated
Left side = Oxygenated
1. Deoxygenated blood is mixed with oxygenated blood.
2. Blood on left side has oxygen saturation decrease from 95% to 80% or lower.
3. Cyanosis may or may not develop depending on how low the oxygen saturation
on the left side drops.
-Left side oxygen saturation 85% or high, cyanosis is not likely to occur.
-Left side oxygen saturation below 80% is indicative of a large amount of blood
being shunted and will result in cyanosis.
Tetralogy of Fallot Most common cyanotic congenital heart defect
Tetralogy of Fallot involves four heart defects:
1. A large ventricular septal defect
2. Pulmonary stenosis
3. Right ventricular hypertrophy
4. An overriding aorta
Heart Failure Risk Factors -Age (most common over 65 y/o)
-Ischemic heart disease
-Obesity
-Diabetes
-Hypertension
-Excessive ETOH use
-Congenital heart disease
-Valvular heart disease
-Myocarditis
-Cardiomyopathy (stiffening of heart muscle)
-Renal failure
Heart Failure Clinical Manifestations -Volume overload
-Poor perfusion secondary to pump failure
